Virus-induced plant diseases in cultivated plants cause important damages in yield. Although the mechanisms of virus infection are intensely studied at the cell biology level, only little is known about the molecular dialog between the invading virus and the host genome. Here we describe a combinatorial genome-wide approach to identify networks of sRNAs-guided post-transcriptional regulation within local Turnip mosaic virus (TuMV) infection sites in Brassica napus leaves. We show that the induction of host-encoded, virus-activated small interfering RNAs (vasiRNAs) observed in virus-infected tissues is accompanied by site-specific cleavage events on both viral and host RNAs that recalls the activity of small RNA-induced silencing complexes (RISC). Cleavage events also involve virus-derived siRNA (vsiRNA)–directed cleavage of target host transcripts as well as cleavage of viral RNA by both host vasiRNAs and vsiRNAs. Furthermore, certain coding genes act as virus-activated regulatory hubs to produce vasiRNAs for the targeting of other host genes. The observations draw an advanced model of plant-virus interactions and provide insights into the complex regulatory networking at the plant-virus interface within cells undergoing early stages of infection.

栽培植物中病毒诱导的植物病害导致产量的重大损失。尽管在细胞生物学水平上对病毒感染的机制进行了深入研究，但对入侵病毒与宿主基因组之间的分子对话知之甚少。在这里，我们描述了一种全基因组组合方法，用于识别甘蓝型油菜中本地芜菁花叶病毒（TuMV）感染位点内的sRNA指导的转录后调控网络。树叶。我们显示，在病毒感染的组织中观察到的宿主编码，病毒激活的小干扰RNA（vasiRNAs）的诱导伴随着病毒和宿主RNA上的位点特异性裂解事件，从而唤起了小RNA诱导的沉默复合物的活性（RISC）。切割事件还涉及病毒衍生的siRNA（vsiRNA）指导的目标宿主转录物的切割，以及宿主vasiRNA和vsiRNA的病毒RNA的切割。此外，某些编码基因充当病毒激活的调节中心，以产生用于靶向其他宿主基因的vasiRNA。这些观察结果绘制了植物病毒相互作用的高级模型，并提供了深入了解感染初期细胞内植物病毒界面复杂调控网络的见解。